The etiological agents of scrapie and transmissible mink encephalopathy are present in high titer in the brains of hamsters and particularly in an inbred line of hamsters. While several methods of purification have not yielded a particle that can be associated with infectivity, study of isolated membrane fractions is continuing based on the hypothesis that the agent is a low molecular-weight nucleic acid contained within a membrane complex. The agent appears to replicate in nerve endings and to be passed in the central nervous system by connecting nerve endings, as it does not replicate in vitro in corneal cultures although it is present in high titer in the cornea of terminally affected hamsters. Mink of the Chediak-Higashi genotype do not develop the spongiform degeneration typical of the disease in normal genotypes. This makes possible study of the mechanisms of the disease process. The susceptibility of mink to mouse purified scrapie and to kuru and Creutzfeldt-Jakob is continuing, as are studies on the host range of TME.